PM2.5-Induced Oxidative Stress and Mitochondrial Damage in the Nasal Mucosa of Rats

Abstract

Exposure to PM2.5 (particulate matter ≤2.5 μm) increases the risk of nasal lesions, but the underlying mechanisms, especially the mechanisms leading to mitochondrial damage, are still unclear. Thus, we investigated the in vivo effects of PM2.5 exposure on the inflammatory response, oxidative stress, the enzyme activities of Na+K+-ATPase and Ca2+-ATPase, and the morphology and function of mitochondria in the nasal mucosa of rats. Exposure to PM2.5 occurred through inhalation of a PM2.5 solution aerosol. The results show that the PM2.5 exposure induced increased levels of malondialdehyde (MDA) and levels of proinflammatory mediators, including interleukin 6 (IL-6), IL-8, and tumor necrosis factor-α (TNF-α). These changes were accompanied by decreases in the activities of total superoxide dismutase (T-SOD), Na+K+-ATPase, and Ca2+-ATPase in rat nasal mucosa. PM2.5 significantly affected the expression of specific mitochondrial fission/fusion genes (OPA1, Mfn1, Fis1, and Drp1) in nasal mucosa. These changes were accompanied by abnormal alterations of mitochondrial structures, including mitochondrial swelling, cristae disorder, and even fission resulting from higher doses of PM2.5. Our data shows that oxidative damage, inflammatory response, and mitochondrial dysfunction may be the toxic mechanisms that cause nasal lesions after exposure to PM2.5.

Nasal epithelial barrier disruption by particulate matter ≤2.5 μm via tight junction protein degradation

“…Excessive ROS exert toxic effects on cellular components via oxidative stress, inflicting direct damage to cell molecules, such as DNA, lipids and proteins, thereby affecting structure and function (Rahal et al, ). Several experimental studies have reported increased ROS production in the respiratory system in response to PM2.5 exposure both in vitro (Deng et al, ; Hong et al, ) and in vivo (Guo, Hong, et al, ). Oxidative damage was also observed in people who have been exposed to PM2.5, as reflected by the formation of 8‐hydroxy‐2′‐deoxyguanosine in urine samples (Wei et al, ).…”

“…PM2.5 was collected from the ceiling (at a height of approximately 20 m) of a five‐story building located at the campus of Fudan University (31.3°N, 121.5°E), Shanghai, China. The study began in November 2014 and ended in April 2015, as described in previous studies (Guo, Dong, et al, ; Guo, Hong, et al, ; Hong et al, ). This site has a mix of industrial, construction, traffic and residential pollutants, and could thereby be considered as a representative sample of the megacity of Shanghai.…”

Mitochondrial fusion, fission, and mitochondrial toxicity

“…Changes in expression patterns of proteins that regulate fusion and fission were observed in rat nasal mucosal tissues after in vivo inhalation of particulate matter (PM 2.5 ) isolated from ambient air samples from Shanghai, China (Guo et al 2017). Mnf1 and Opa1 mRNA and protein expression were increased at low and medium doses of PM 2.5 (200 and 1000 μg/m 3 ), potentially compensating for damage or in response to increased energy demands, but decreased at a high dose PM 2.5 (3000 μg/m 3 ).…”

Zearalenone induces ROS‐mediated mitochondrial damage in porcine IPEC‐J2 cells

“…As we all know, mitochondria, as the unique double‐membrane subcellular organelles, provide body energy and participate in metabolic and genetic functions. Mitochondrial damage will induce the cell death even organ injury . However, to the best of our knowledge, the information about mitochondrial damage induced by ZEA via ROS has not been reviewed.…”